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Diffuse midline gliomas (DMGs) with the histone H3 K27M mutation are fatal pediatric tumors. In this issue, Michelle Monje and colleagues report that CAR T cells targeting the disialoganglioside GD2 are capable of killing DMG cells in preclinical models, offering hope for clinical translation of this immunotherapy. The cover depicts a tiger attacking hyenas, which do not naturally coexist in the same geographic region, to represent an exogenously introduced CAR T cell attacking glioma cells.
For more than two decades, Nature Medicine has been the prime venue for publication of outstanding work in the translational space. Now the journal’s scope is evolving to embrace the clinical research that meets the challenges and complexities of contemporary medicine.
Anti-GD2 chimeric antigen receptor (CAR)-modified T cells may be a new and innovative approach for the treatment of pediatric H3-K27M-mutant diffuse midline gliomas.
In triple-negative breast cancer, therapeutic response to carboplatin and docetaxel is similar. However, carboplatin therapy is superior to docetaxel in patients with germline BRCA1 or BRCA2 mutations, but ‘BRCAness’ does not predict sensitivity to carboplatin.
A crucial role for glucose metabolism has been identified in wound repair and in the pathogenesis of chronic inflammatory skin diseases, indicating that targeting metabolism is an approach for treating psoriasis.
An artificial intelligence (AI) using a deep-learning approach can classify retinal images from optical coherence tomography for early diagnosis of retinal diseases and has the potential to be used in other image-based medical diagnoses.
The tumor immune microenvironment influences tumor progression and response to immunotherapy; its further characterization will improve therapeutic outcome.
Treatment with setmelanotide, a new-generation MC4R agonist, provides durable weight loss in hyperphagic, leptin receptor–deficient patients, suggesting a pharmacological avenue to treat patients with various MC4R pathway defects.
An IL-6/STAT3 signature and memory CD8 T cell subset in preinfusion chimeric antigen receptor–expressing T cells associate with response in patients with high-risk chronic lymphocytic leukemia.
Lethal pediatric tumors bearing a particular histone H3 mutation upregulate the disialoganglioside GD2, thereby making these tumors susceptible to chimeric antigen receptor T cell–based immunotherapy.
The transcription factor ELK-1 is upregulated in patients with major depressive disorder, and selective inhibition of hippocampal ELK-1 produces rapid antidepressive effects in rodent models of depression.
Expression of PM20D1 is regulated by long-range chromatin interactions with an Alzheimer’s disease risk haplotype, and PM20D1 overexpression reduces AD-like pathology and cognitive impairment in a rodent model.
A shared gene expression program associated with silencing HIV-1 transcription may be critical for persistence of reactivated latent CD4+ T cells in patients with HIV.
Keratinocytes require glucose for injury- or inflammation-driven but not homeostatic proliferation, and glucose-transport blockade blocks psoriasis-like pathology in experimental models.
The phase 3 TNT Trial in subjects with triple-negative breast cancer supports the superiority of carboplatin over docetaxel in BRCA1/2-mutated tumors and a greater response to taxanes in the nonbasal subtype.
Human iPSC-derived neurons are generated from individuals with or without Alzheimer's disease carrying different APOE alleles and reveal a toxic, neuron-intrinsic gain of function of the ApoE4 variant that is a strong genetic risk factor for AD.
In mouse models of stress-induced depression, molecular and chemogenetic stimulation of the entorhinal cortex induces the production of adult-born hippocampal neurons and generates antidepressive-like effects.
Promoting more bone growth is of keen interest in the treatment of osteoporosis, and preventing the degradation of S1P offers a new therapeutic avenue for this approach.
Comprehensive integration of mutational and structural alterations in clinically-annotated DLBCL patient samples provides a novel molecular classification of the disease.